By Maria M. Picken MD PhD FASN, Ahmet Dogan, Guillermo A. Herrera
ISBN-10: 3319192930
ISBN-13: 9783319192932
ISBN-10: 3319192949
ISBN-13: 9783319192949
The moment variation of this article provides an outline of the newest advancements during this region together with medical presentation, etiology, pathogenesis, and differential prognosis. the reason for varied remedies, together with transplantation, is mentioned and tissue prognosis (its pitfalls and techniques for heading off them) and laboratory aid are incorporated. The involvement of all significant organ structures together with renal/genitourinary, cardiac, gastrointestinal, pulmonary, peripheral nerve/central apprehensive process, tender tissue, dermis, lymph node/spleen and bone marrow pathology can also be covered.
Amyloid and comparable problems, moment Edition may be important to really expert and normal pathologists in addition to cytopathologists. different doctors can also take advantage of this concise replace at the systemic amyloidoses.
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Sample text
Nat Rev Mol Cell Biol. 2007;8:101–12. 60. Glabe CG. Structural classification of toxic amyloid oligomers. J Biol Chem. 2008;283:29639–43. 61. Stefani M. Structural polymorphism of amyloid oligomers and fibrils underlies different fibrillization pathways: immunogenicity and cytotoxicity. Curr Protein Pept Sci. 2010;11:343–54. 62. Serio TR, et al. Nucleated conformational conversion and the replication of conformational information by a prion determinant. Science. 2000;289:1317–21. 63. Knowles TP, et al.
Conduction disturbances are also frequently observed and negatively influence prognosis [198, 199]. Despite the great impact of cardiac involvement on prognosis, an effective treatment can significantly improve the survival of AL patients with cardiac amyloidosis, thus radically modifying the natural history of the disease [200]. Approximately, 22 % of AL patients present with liver involvement, resulting in hepatomegaly and/or elevated serum alkaline phosphatase levels [174, 201]. Jaundice is rare and, when present, often indicates a poor prognosis [202– 204].
Ameliorate protein misfolding diseases. Curr Opin Chem Biol. 2013;17:346–52. Westermark GT, Westermark P. Serum amyloid A and protein AA: molecular mechanisms of a transmissible amyloidosis. FEBS Lett. 2009;583:2685–90. Corlin DB, Heegaard NH. Beta(2)-microglobulin amyloidosis. Subcell Biochem. 2012;65:517–40. Abrahamson M, Grubb A. Increased body temperature accelerates aggregation of the Leu-68→Gln mutant cystatin C, the amyloid-forming protein in hereditary cystatin C amyloid angiopathy. Proc Natl Acad Sci USA.
Amyloid and Related Disorders: Surgical Pathology and Clinical Correlations by Maria M. Picken MD PhD FASN, Ahmet Dogan, Guillermo A. Herrera
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